Chronic Exercise-Induced Leg Pain in Active People More Than Just Shin Splints

Lew C. Schon, MD

Donald E. Baxter, MD

Thomas 0. Clanton, MD

Foot and Ankle Series Editor: G. James Sammarco, MD

"Shin splints" is a catchall term for any kind of persistent exer­cise-related lower leg pain with no

obvious cause. Such pain can originate from a number of conditions, such as medi­al tibial stress syndrome, stress fracture, compartment syndrome, vascular patholo­gy, nerve entrapment, and others. A me­thodical work-up designed to detect prob­lems in all anatomic structures from bone to skin will narrow the possibilities and lay the basis for appropriate treatment.

1 o most people, physicians and patients alike, persistent lower leg pain related to exercise means "shin splints." This term includes many conditions that must be

considered when evaluating chronic exercise-in­duced leg pain in active individuals. Injuries may affect every anatomic structure in the leg: bones,

continued

Dr Schon is an attending orthopedic surgeon at Union Memorial Hospital in Baltimore. In addition, Dr Schon,is a clinical instructor of orthopedics, Dr Baxter is a clinical asso­ciate professor of orthopedics, and Dr Clanton is a clinical assistant professor of orthopedics at the University of Texas Health Science Center at Houston School of Medicine. Dr Baxter is also director of the foot and ankle fellowship at the same school, and is a clinical associate professor of ortho­pedics at the Baylor College of Medicine in Houston. Dr Sammarco is an orthopedist with the Center for Orthopedic Care, Inc, in Cincinnati and a consulting physician to the University of Cincinnati Department of Athletics and the Cincinnati Ballet Company. He is a member of the editorial board of THE PHYSICIAN AND SPORTSMEDICINE and a member of

the American College of Sports Medicine. Drs Baxter, Clan­ton, and Sammarco are fellows of the American Orthopedic Foot and Ankle Society.

If repetitive impact causes leg pain, patients may need to glide into a different sport.

*ss»

:•....:....., ••••.. ;

^.r^v"-' <ft:;:i

100 Vol 20 • No. 1 • January 92» THE PHYSICIAN AND SPORTSMEDICINE : THE PHYSICIAN

id Leg

Photo: © 1992. Caroline Wood/F-Stock

• ". • . . . '

'.:•:•: • . .. . • • .. • If :'•'• V;; ,.v v ^ ' ; '

IAN AND SPORTSMEDICINE

leg pain continued

Photos: © 1992. Courtesy of Lawrence Holder, MD, Union Memorial Hospital, Baltimore.

Figure 1. Medial tibial stress syndrome of a young, male adult runner. Lateral (a) and anteroposterior (b) views of a patient by technetium bone scan show diffuse linear uptake along the posteromedial cortex of the tibia (arrows).

Figure 2. Medial tibial stress fracture of a young, male adult runner. Anteroposterior (a) and lateral (b) technetium bone scan views showing localized intense uptake along the posteromedial border of the midtibia (arrows).

compartments, muscles, tendons, ligaments, fascia, arteries, veins, nerves, and skin. The dif­ferential diagnosis of chronic exercise-induced leg pain, therefore, should include medial tibial sttess syndrome, stress fracture, chronic com­partment syndrome, muscle strain, muscle her­niation, tendinitis, fasciitis, arterial insufficiency venous pathology, nerve entrapment, and ra-

102

diculopathy—each, of course, with a variety of expressions.

To complicate the picture, several conditions may coexist. A history, a physical examination, and an observation of the patient peiforming the pain-causing activity are needed to establish an accurate diagnosis. The eight injuries most diffi­cult to diagnose are detailed below.

Medial Tibial Stress Syndrome The etiology of medial tibial stress syndrome

is open to debate. Although some contend that the pain relates to periostitis underneath the posterior tibialis muscle, more recently others have implicated the investing fascia of the soleus as it inserts on the posterior medial tibia. Most agree that the syndrome is caused by a stress reaction of the fascia, periosteum, or bone—or a combination of these—along the posteromedial aspect of the tibia. These in­creased stresses on the fascia and periosteum may result from abnormal pronation, excessive subtalar motion, or both.1-2

A study by Clement et al3 of 1,819 common running injuries affecting all parts of the body reported 239 cases (13.1%) of tibial stress syn­drome, making it the second most common in­jury in the study. Detmer4 described three caus­es of medial tibial stress syndrome: Type I is a stress reaction or fracture of the bone, type II in­dicates a chronic periosteal elevation from the bone secondary to too much pull from the soleus fascia, and type IH is a posterior or isolat­ed posterior tibialis compartment syndrome.

Patients who develop medial tibial stress syn­drome report recurrent discomfort along the medial border of the middle and distal tibia. This pain is exacerbated by exercise and incomplete­ly relieved by rest. In particular, running on banked indoor tracks or uneven tenain can in­duce the syndrome.

Physical examination reveals tenderness along the posteromedial border of the tibia. Oc­casionally, local induration is noted, but any neurologic or vascular abnormalities rule out tibial stiess syndrome. Pronation and excessive subtalar range of motion are common.

Although radiographs frequently are normal, a bone scan may demonstrate diffuse linear up-

continued Vol 20 • No. 1 • January 92 • THE PHYSICIAN AND SPORTSMEDICINE

m

m

WooH itrolfi m9 9«jf§

lendejjfl ince -;"

leg pain continued

; . ! «

St

I P

/Ith a l p Inn, ail' •ciiiiilej' ion,:* '»;»/«•• :i*nt> lemla;.:| breasIB

JmisllSii 'ySilffl

inowil eallnlH nwfl.F

rals,;fj irfiidiK

IDUM flvldiElif irtfiL sed tt|a

inceta ibo.1

inslir

«J§

I N o l l

take along the posteromedial border of the tibia involving one third of the bone's length (figure l).s

Pressure studies of the suspected compartments before and after exercise will help identify a deep posterior or posterior tibialis compartment syn­drome or rule out concurrent anterior compart­ment syndrome.

Treatment of medial tibial sttess syndrome consists of rest followed by a gradual return to ac­tivity Achilles tendon stretches, heel pads, casts, local steroid injections, and taping have been used with varying success. Athletes who over-pronate or have abnormal subtalar mobility and who don't heal after relative rest, may be fitted with orthotics. If conservative modalities fail, a posteromedial fasciotomy releasing the medial soleus fascia and deep posterior compartment may be warranted.1

Tibial or Fibular Stress Fracture Stress fractures develop when repetitive loads

cause bones to resorb more than they form. Physicians often see stress fractures in runners. Clement et al's study3 of common overuse in- ing. juries reported 47 (2.6%) tibial stress fractures. It was the eighth most prevalent running injury in the study. These fractures also occur regularly in basketball, soccer, dancing, and skating. Athletes who have smaller diameter bones, less cortical bone, or diminished bone mineral content are at increased risk for stress fractures. (See "Repeated Stress Fractures in an Amenorrheic Marathon-er," April 1989, page 65.)

Typically, an athlete who sustains a stress fracture will report a recent change in routine, running surface, or shoes. Frequently, symp­toms crescendo over the course of several weeks, but in rare cases they occur quite suddenly The pain initially may be diffuse, but with time it be­comes localized. Impact activities such as jump­ing will exacerbate symptoms.

An athlete who has a stress fracture may have local bony tenderness associated with indura­tion of the overlying soft tissues. Increased warmth and even erythema may also be pre­sent. Some patients may have a tender, firm mass over the fracture site. Tapping or stressing the bone may elicit pain at the fracture site.

Radiography may not show changes for 2 or

T H E PHYSIC IAN A N D S P O R T S M E D I C I N E • Vol 20 • No. 1 • January 92

more weeks and in some cases may never reveal the fracture. The first sign of a stress fracture of­ten will be a faint localized radiopaque haze. In time, a small cortical lucency and a more estab­lished periosteal reaction may appear. In cases of longer duration, cortical lucencies may tra­verse the bone.

Although magnetic resonance imaging (MRT) may be more sensitive than other studies for detecting a stress fracture early, technetium bone scanning remains the diagnostic modality of choice. The characteristic finding in a stress fracture is intense local activity with a fusiform accumulation of tracer (figure 2).

Treatment involves rest and avoid­ance of the offending stresses. Al­though immobilization is rarely neces­sary, weight bearing is not advisable. Once the pain has diminished, the pa­tient can resume weight-bearing activ­ities as tolerated. During recuperation, athletes can cross-train to maintain cardiovascular and muscle condition-

Typically, an athlete Who sustains a stress fracture will report a recent 'change in routine, running surface, or footwear.

Anterior tibial stress fractures have the worst prognosis and are the most challenging to treat. If patients' x-rays showradi-olucencies—and especially if diminished ra­dionuclide uptake is also evident by technetium bone scan—there is a risk of delayed union or complete fracture (figure 3).6 Rettig et al7 recom­mend treating these fractures with pulse electro­magnetic fields 10 to 12 hours a day for at least 3 to 6 months. They suggest that if the fracture has not healed by that time, a bone graft may be considered.

Based on a study in which five of six athletes went on to develop a complete fracture, Green et al" recommend excision and bone graft for ante­rior tibial stress fractures that do not heal in 4 to 6 months. These six were not initially treated with electromagnetic fields; there is consider­able controversy over using pulse electromag­netic fields in these cases. Further investigation is needed to establish the fields' efficacy

Chronic Compartment Syndrome Chronic compartment syndrome is caused

by elevated intracompartmental pressures re-continued

105

I?;'III!

i l

II

m 1 19 1 I'll 11 ill 1

M

il! J E I I I C

leg pain continued

Figure 3. A male collegiate triple jumper's chronic symptomatic stress fracture of the anterior tibia (arrows): anteroposterior (a) and lateral (b) views.

suiting in ischemia of muscles and nerves. Ele­vated pressure may occur when exercise couples relatively rigid fascial boundaries with the in­creased muscle bulk caused by muscle contrac­tion, intra- and extracellular fluid accumulation, and hemorrhaging microtears of the muscle. Ve­nous and lymphatic compromise exacerbate the situation.

Although a physician specializing in athletic

106

injuries to the lower extremity may see such pa­tients with some frequency, the prevalence of this condition in the general population is low. In one study,3 chronic compartment syndrome was diagnosed in 3 patients over the course of a year among a university population of 4,000.

Typically, athletes who have chronic com­partment syndrome will have pain when they run a certain distance, speed, or duration. A few minutes to several hours of rest will usually alle­viate discomfort. The pain is characterized as aching, cramping, or stabbing. The patient will often report a sensation of fullness in the leg over the involved compartments. Occasionally an athlete will report shooting pains, numbness, tingling, and burning in the leg, ankle, or foot along the nerve that runs through the compart­ment. Involvement of both legs is common, but simultaneous involvement is less frequent than asynchronous presentation. About 15% to 20% of patients will report a recently diagnosed stress fracture.9

Physical examination may be completely normal, but if a patient's leg is stressed before the evaluation, swelling in the affected compart­ment may be noted. Muscle hernias may be found in 20% to 60% of patients,10" and neuro­logic abnormalities may occasionally be found. Radiographs are usually normal, but a tech­netium bone scan may occasionally reveal sub­tle changes that usually signify coexistent medial tibial stress syndrome or stress fracture.

Compartmental pressure monitoring with a wick catheter before, during, and after exercise will help confirm the diagnosis, though preexer-cise and postexercise pressures maybe sufficient. The diagnosis is supported by compartmental pressures that do not return to baseline after 5 minutes and are greater than 15 mm Hg at rest, greater than 50 to 70 mm Hg while exercising, and greater than 30 mm Hg after exercise2

Treatment begins with rest and reduction of the duration and intensity of activities. Then a gradual increase in exercise in conjunction with ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and orthotic devices may work. Often, however, these measures fail to control the pain, and a fasciotomy of the involved compartment is warranted. (See "Chronic Compartment Syn-

continued Vol 20 • No. 1 • January 92 • THE PHYSICIAN AND SPORTSMEDICINE

•a

leg pain coi

drome: Surgic 1991, page 63, successful, J swelling, new persistent low of which may

Gastrocnem A gastrocm

in racket sporl the past, this tails muscle r generally acce taris rupture two cases in • rupture has a cause of its p. players.

The injury their knees fie ion, and then in jumping.14'; tracted muscle

Athletes wl experience su< varying degre Typically, the someone kick aching pain n severity of the. swelling are m walk and plani swelling and o middle third o ate strains. Tyj their toes beca juries, there n loss of gastrocr

A program taping and in i ing, will often stretches folio1

added once tht With mode

brace may be i flexion. Some j or brace with tl tar flexed. Onc< be removed. A

THE PHYSICIAN AN

i see such pa-prevalence of olation is low. art syndrome tie course of a i of 4,000. :hronic com-in when they trration. A few 11 usually alle-iracterized as le patient will ess in the leg Occasionally,

is, numbness, ankle, or foot the compart-common, but frequent than it 15% to 20% ignosed stress

e completely lessed before cted compart-rnias may be 011 and neuro-ally be found. 1, but a tech-dly reveal sub-xistent medial ;ture. litoring with a . after exercise lough preexer-iy be sufficient. )mpartmental baseline after mmHg at rest, tile exercising, xercise.2

d reduction of rtivities. Then i conjunction imatory drugs ly work. Often, mtrol the pain, compartment partment Syn-

contihued SPORTSMEDICINE

f

leg pain continued

drome: Surgical Intervention in 12 Cases," April 1991, page 63.) Although surgical release is often successful, some athletes may experience swelling, new muscle herniations, nerve injuries, persistent low-grade pain, and recurrence—any of which may limit a patient's ability to exercise.

Gastrocnemius Rupture A gastrocnemius rupture or strain may occur

in racket sports, basketball, running, or skiing. In the past, this lesion was believed to be a plan­taris muscle rupture. However, this diagnosis is generally accepted as obsolete because a plan­taris rupture was documented in only one or two cases in the literature.1213 Gastrocnemius rupture has also been called "tennis leg" be­cause of its prevalence in middle-aged tennis players,

The injury occurs when athletes crouch with their knees flexed and their ankles in dorsiflex­ion, and then suddenly extend their knees—as in jumping.14 This eccentric loading of the con­tracted muscle causes the rupture.

Athletes who have a gastrocnemius rupture experience sudden, severe calf pain followed by varying degrees of swelling and ecchymosis. Typically, they report that the pain feels like someone kicked them in the leg. Cramping or aching pain may continue depending on the severity of the injury. With mild strains, pain and swelling are minimal, and the patient is able to walk and plantar flex the ankle. A fair amount of swelling and occasionally a palpable gap in the middle third of the muscle accompany moder­ate strains. Typically, patients cannot stand on their toes because of pain or spasm. In severe in­juries, there may be a large, palpable gap and loss of gastrocnemius or soleus function.

A program of rest and icing, with or without taping and in conjunction with passive stretch­ing, will often heal a mild strain. Standing calf stretches followed by strengthening should be added once the pain has cliiTiinished.115

With moderate strains, a short leg cast or brace may be applied with the ankle in plantar flexion. Some patients may need a long leg cast or brace with the knee flexed and the ankle plan­tar flexed. Once the pain decreases, the cast may be removed. A heel lift, with or without taping of

THE PHYSICIAN AND SPORTSMEDICINE • Vol 20 • No. 1 • January 92

Photo: a 1992. David Madison

wMiKwSMBs

',''•':•'•'•':•' • ' '• .•'•'

Skaters and other athletes who develop muscle fatigue may need to give relative rest a whirl.

the leg in equinus, may then be beneficial. When passive stretching is tolerable, the patient may begin calf stretches followed by strengthening exercises.

For severe strains, the best course is conser­vative treatment with or without long leg casting, followed by reasonably aggressive physical ther­apy. Miller14 advocates an operative approach with drainage of the hematoma, debridement, and apposition of the muscle. We have under­taken a retrospective review, still unpublished, that indicates that disability following moderate and severe ruptures may last several months and, occasionally, manyyears.

Muscle Overuse Eccentric contractions during exercise fre­

quently produce delayed-onset muscle pain, fa­tigue, stiffness, and tenderness. Symptoms may last several days. Treatment includes relative rest, cross-training, and avoidance of hill run­ning. Further work-up and treatment are based

continued 111

leg pain continued

Photo; © 1992. Lew C. Sohon

Figure 4. A 34-year-old female runner who has superficial peroneal nerve entrapment with fascial defect and muscle herniation (arrows) at the site of nerve penetration in the anterolateral aspect of the lower leg. The bulge is typically located 10 to 12 cm above the end

on die clinician's suspicion of other processes being at work.!6'17

External Iliac Arterial Occlusion Chevalier et al1" describe an uncommon syn­

drome of endofibrosis of die external iliac artery in bicycle racers. The athletes complain of a par­alyzing pain in tiieir legs occurring with maximal effort. They typically have descending painful muscle contractions in the calf with subsequent diminished sensory and motor responsiveness of the extremity. A few minutes alter the cyclist returns to normal speed, the pain subsides,

Physical examination performed with the pa­tient at rest may yield normal findings. Thigh and calf circumference may be larger in die af­fected extremity, but when the tiiigh is maximal­ly flexed, a systolic bruit may be auscultated in

112 v

the femoral triangle. Bicycle stress tests with Doppler ultrasound systolic pressures at die an­kle may show decreased pressures when symp­toms are present. Angiography may show a stenotic lesion in the external iliac artery.

Treatment depends on die athlete's dedica­tion to cycling, because avoiding the threshold intensity will prevent recurrence. Chevalier et al1" say competitive cyclists may need endarterecto-my and shortening of the artery.

Venous Pathology Venous insufficiency, thrombosis, or throm­

bophlebitis may occur as isolated conditions or in association with acute and chronic leg injuries. Risk factors include: (1) severe muscle or bone injury (eg, fracture, complete muscle rupture, contusion), (2) immobilization following a lower extremity injury, (3) prolonged inactivity (per­haps during transportation to athletic events), (4) high altitude, (5) dehydration, (6) alcohol or otiier drug abuse, (7) estrogen supplementation (eg, birth control pills), and (8) hemoglobinopathies (eg, sickle cell anemia).

Patients who have pain, swelling, and diffuse calf tenderness may have venous pathology and should be evaluated with noninvasive flow tests or venography. In our unpublished retrospective review, two patients with exercise-induced leg pain had severe venous sequelae. Both patients had classic histories of gastrocnemius rupture. One patient developed a superficial femoral vein thrombosis, and the other had a pulmonary em­bolism.

Treatment of a deep venous thrombosis usu­ally requires anticoagulation with heparin sodi­um and then warfarin sodium. (See "Effort Thrombosis in a Runner," June 1990, page 76.) Superficial thrombophlebitis in die calf may be heated with elevation, compresses, rest, aspirin, and frequent observation. And compression stockings may improve venous insufficiency.

Nerve Entrapment A final cause of exercise-induced leg pain

may be nerve entrapment. In our experience, entrapment most commonly involves the su­perficial peroneal nerve (figure 4). Entrapment is consistently located where the nerve penetrates

continued l 20 • No. 1 • January 92 • THE PHYSICIAN AND SPORTSMEDICINE

leg pain continued

*

the fascia and sometimes results from pressure caused by a muscle hernia. Other areas of en­trapment include the common peroneal nerve in the region of die fibular neck, the posterior tibial nerve in the popliteal fossa or tarsal tunnel, the saphenous nerve as it pierces Hunter's canal, and the sural nerve in the calf.1922

Patients will often have vague, diffuse pain. Occasionally, they may have neuritis with burn­ing, tingling, shooting, or radiating pain. Direct­ed questioning will help isolate the discomfort, which often lies along the involved nerve. Local­ized nerve tenderness at the point of compres­sion is characteristic. Percussion or prolonged pressure at this point usually reproduces the pain. It's also important to exclude the possibility of a coexisting chronic compartment syndrome or a more proximal nerve entrapment.

Conservative treatment consists of injections, massage, relative rest, NSAIDs, and shoe modifi­cations. When these measures are unsuccessful,

release of the nerve with a localized fasciotomy may be warranted.

Customized Care When an active person experiences chronic

exercise-induced lower leg pain, the differential diagnosis includes chronic compartment syn­drome, medial tibial stress syndrome, stress frac­ture, gastrocnemius rupture, muscle overuse, external iliac arterial occlusion, venous patholo­gy, and nerve entrapment. Fortunately, these in­juries are minor if detected and treated properly. To make an accurate diagnosis, physicians need to know the natural history of each condition. They can then customize treatment for each pa­tient's sport and long-term goals. KM

Address correspondence to Lew C. Schon, MD, Union Memorial Hospital, 201 E University Plcwy, Baltimore, MD 21218.

References 1. -Michael'RHy'Holder-LE:' The soleus syndrome: a

cause of medial tibial stress (shin splints). Am J Sports Med 1985;13(2):87-94

2. Viitasalo JT, Kvist M: Some biomechanical aspects of the foot and ankle in athletes with and without shin splints. Am J Sports Med 1983;11 (3): 125-130

3. Clement DB, Taunton JE, Smart GW, et al: A survey of overuse running injuries. Phys Sportsmed 1981; 9(5):47-58

4. Detmer DE: Chronic shin splints: classification and management of medial tibial stress syndrome, Sports Med 1986;3(6):436-446

5. Holder LE, Michael RH: The specific scintigraphic pattern of "shin splints in the lower leg": concise communication. I Nucl Med 1984;25(8):865-869

6. Blank S: Transverse tibial stress fractures: a special problem. Am J Sports Med 1987;15(6):597-602

7. Rettig AC, Shelbourne ICD, McCarroll JR, et al: The natural history and treatment of delayed union stress fractures of the anterior cortex of the tibia, Am J Sports Med 1988;16(3):250-255

8. Green NE, Rogers RA, Lipscomb AB: Nonunions of stress fractures of the tibia. Am J Sports Med 1985; 13(3).T71-176

9. Detmer DE, Sharpe K, Sufit RL, et al: Chronic com­partment syndrome: diagnosis, management and outcomes. Am I Sports Med 1985;13(3):162-170

10. Mubarak SI, Hargens AR: Exertional compartment syndromes, in Mubarak SJ, Hargens AR (eds): Com­partment Syndromes and Volkmann's Contracture. Philadelphia, WB Saunders Co, 1981

11. Reneman RS: The anterior and lateral compartmen­tal syndrome of the leg due to intensive use of mus-

12

13,

cles. Clin Orthop 1975;Nov-Dec(ll3):69-80 Mennen U: Rupture of the plantaris: does it exist?, letter. J Bone Joint Surg (Am) 1983;65(7):1030 Severance HW Jr, Bassett FH 3rd: Rupture of the • plantaris: does it exist? J Bone Joint Surg (Am) 1982; t 64(9): 1387-1388 §

14. Miller WA: Rupture of the musculotendinous junc­ture of the medial head of the gastrocnemius mus­cle. Am J Sports Med 1977;5(5):191-193

15. Miller AP: Strains of the posterior calf musculature ("tennis leg"). AmJSports Med 1979;7(3):172~174

16. Armstrong RB: Mechanisms of exercise-induced de­layed-onset muscular soreness: a brief review. Med Sci Sports Exerc 1984:16(6) :529-538 Friden J, SfaManos PN, Hargens AR, et al: Residual muscular swelling after repetitive eccentric contrac­tions. J Orthop Res 1988;6(4):493-498 Chevalier JM, Enon B, Walder J, et al: Endofibrosis of the external iliac artery in bicycle racers: an unrec­ognized pathologic state. Ann Vase Surg 1986; 1(3): 297-303 Mozes M, Ouaknine G, Nathan H: Saphenous nerve entrapment simulating vascular disorder. Surgery 1975;77(2):299-303

20. Schon LC, Baxter DE: Neuropathies of the foot and ankle in athletes. Clin Sports Med 1990;9(2):489-509

21. StyfJ: Entrapment of the superficial peroneal nerve: diagnosis and results of decompression. J Bone Joint Surg (Br) 1989;71(1):131-135

22. Worth RM, Kettelkamp DB, Defalque RJ, et al: Saphenous nerve entrapment: a cause of medial knee pain. Am J Sports Med 1984;12(1):80-81

17

18

19

114 Vol 20 • No. 1 • January 92 • THE PHYSICIAN AND SPORTSMEDICINE